Atopic dermatitis (AD) also known as atopic eczema or eczema[1] is a type of dermatitis, an inflammatory, relapsing, non-contagious and itchy skin disorder.[2] It is often chronic in nature.[3] In children under one year of age much of the body may be affected.[3] As they get older the back of the knees and front of the elbows are the most common area for the rash.[3] In adults the hands and feet are most affected.[3]

Treatment involves: avoiding things that make it worse, daily bathing with use of a moisturising cream afterwards, steroid creams when flares occur, and medications to help with itchiness.[3] Antibiotics (either by mouth or topically) may be needed if infections develop.[3]

It affects more than 10% of children in the United States and is more common in younger children.[3] Most people outgrow it.[3] It has been given names like "prurigo Besnier," "neurodermatitis," "endogenous eczema," "flexural eczema," "infantile eczema," and "prurigo diathésique".[4]

People with AD often have dry and scaly skin that spans the entire body, except perhaps the diaper area, and intensely itchy red, splotchy, raised lesions to form in the bends of the arms or legs, face, and neck.[5][6][7][8][9] These lesions then weep, crack, swell, and crust over.[9] These lesions are at a heightened risk for bacterial, fungal, or viralcolonisation.[9]

The cause of AD is not known, although there is some evidence of genetic factors, and some evidence that growing up in a sanitary environment encourages AD.[6]

It seems to have a genetic component. Many people with AD have a family history of atopy. Atopy is an immediate-onset allergic reaction such as asthma, food allergies, AD or hay fever.[5][6] In 2006 it was discovered that mutations in the gene for the production of filaggrin strongly increased the risk for developing atopic dermatitis. Most importantly two mutations were found that affect approximately 5% of people in Western Europe that may disrupt the production of filaggrin. Filaggrin is a protein that plays an important role in the retention of water in the stratum corneum. People who have these mutations often have dry skin.[10] Filaggrin also plays an important role in keeping the skin surface slightly acidic, hence giving it anti-microbial effects. It is broken down into trans-urocanic acid which keeps the pH low.[11]

According to the hygiene hypothesis, when children are brought up exposed to allergens in the environment at a young age, their immune system is more likely to tolerate them, while children brought up in a modern "sanitary" environment are less likely to be exposed to those allergens at a young age, and, when they are finally exposed, develop allergies. There is some support for this hypothesis with respect to AD.

Those exposed to dogs while growing up have a lower risk of atopic dermatitis.[12] There is also support from epidemiological studies for a protective role for helminths against AD.[13] Likewise children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurised milk.[13] Exposure to dust mites is believed to contribute to one's risk of developing AD.[14]

A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems to be true for fast foods.[13]

The atopy patch test, which has been recognized as a useful diagnostic tool, involves the application of intact protein allergens in a patch test setting with an evaluation of the induced skin lesions after 24 to 72 hours, in an effort to determine if a specific allergen is causing the symptoms.[15][16]

There is no known cure for AD, although treatments may reduce the severity and frequency of flares.[5] Applying moisturisers may prevent the skin from drying out and decrease the need for other medications.[17] Affected persons often report that improvement of skin hydration parallels with improvement in AD symptoms.[5] Additionally topical corticosteroids, especially hydrocortisone have proven themselves effective in managing AD.[5][6] If topical corticosteroids and moisturisers fail, short-term treatment with topical calcineurin inhibitors like tacrolimus or pimecrolimus may be tried, although they are usually avoided as they can cause skin cancer or lymphoma.[5] Alternatively systemic immunosuppressants may be tried such as ciclosporin, methotrexate, interferon gamma-1b, mycophenolate mofetil and azathioprine.[5][18] Antidepressants and naltrexone may be used to control pruritus (itchiness).[19]

A more novel form of treatment involves exposure to broad or narrow-band ultraviolet light. UV radiation exposure has been found to have a localized immunomodulatory effect on affected tissues and may be used to decrease the severity and frequency of flares.[20][21] In particular, Meduri et al. have suggested that the usage of UVA1 is more effective in treating acute flares, whereas narrow-band UVB is more effective in long-term management scenarios.[22] However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.[23] Vitamin D has also proven itself an effective treatment for AD.[24]

It is often recommended that persons with AD bathe regularly in lukewarm baths, especially in salt water, in order to moisten their skin.[6][25] Avoiding woollen clothing is usually recommended for those with AD, likewise silk, silver-coated clothing is often recommended as a therapeutic measure against AD.[25] Dilute bleach baths have also been reported effective at managing AD.[25]

Since the beginning of the twentieth century, many mucosal inflammatory disorders have become more common; atopic eczema (AE) is a classic example of such a disease. It now affects 15–30% of children and 2–10% of adults in developed countries and in the United States has nearly tripled in the past thirty to forty years.[6][26]